Ossification And Bone Disease Flashcards
(40 cards)
What is the process of endochondral ossification?
Initially whole bone is cartilage. As embryo, collar of periosteal bone appears in shaft (around the edge). As foetus, the central cartilage calcifies and becomes primary centre (in diaphysis). nutrient artery penetrates supplying osteogenic cells. primary ossification. Post natal, Medulla becomes cancellous bone, cartilage forms epiphysial growth plates. Epiphyses develop secondary centres of ossification. Prepubertal, Epiphyses ossify and grow plates move apart, lengthening bone. Mature adult, epiphyseal growth plates replaced by bone (mineralised to become bone). Hyaline cartilage only at articulating surfaces.
What are the different zones that form from the growth plate in endochondal ossification?
Zone of reserve cartilage- no cellular proliferation or active matrix production.
Zone of proliferation- chondrocytes actively dividing it form columns, cells enlarge and secrete matrix.
Zone of hypertrophy- cells enlarge greatly. Matrix compressed into linear bands between cell columns.
Zone of calcified cartilage- enlarged cells begin to degenerate and matrix calcifies.
Zone of resorption- calcium matrix in direct contact with marrow cavity. Small blood vessels and connective tissue invade region occupied by dying chondrocytes leaving the calcified cartilage as spicules between them. Bone is laid down on the cartilage spicules.
What is an osteoid?
Non calcified (mineralised) bone
Why do osteoclasts have lots of nuclei?
They are phagocytic and were formed from merging of a few macrophages.
In what way too bones grow by endochondral ossification?
Increase in lengths he to the epiphyseal growth plates. Grow in diameter by deposition of bone at periphery of shaft (intramembranous)
What bones develop by endochondral ossification?
Long bones
What happens to the cartilage in the growth plate prior to endochondral ossification?
Columns of cartilage extend from the growth plate
What happens in intramembranous ossification?
Development starts in highly vascularised connective tissue. This focus of activity is primary centre. Mesenchymal cells differentiate into osteoblasts which are surrounded by collagen fibres and ground substance. The osteoblasts secrete uncalcified matrix (osteoid) which layer becomes calcified and forms rudimentary spicules. Osteoblasts become osteocytes (entombed in osteoid). Spicules joint to form trabeculae which merge to form woven bone. Finally replaced by lamellae of mature compact bone.
What is formed initially in intramembranous ossification and what does this become?
Spongy bone which is then transformed to compact bone.
How does the structure of bone constantly change?
By bone resorption and bone remodelling.
What types of bones have intramembranous ossification?
Flat bones eg skull
Also thicken long bones
What causes osteogenesis imperfecta?
Autosomal dominant group of disorders of connective tissue caused by mutation in gene for type 1 collagen. Therefore abnormal collagen synthesis by osteoblasts and fibroblasts.
What is osteogenesis imperfecta characterised by?
Bone fragility (predisposes sufferer to fractures and deformity), abnormalities of eyes, ears, teeth, joints, skin, skeleton.
What can multiple fractures due to osteogenesis imperfecta be confused with?
Deliberate injury
what happens in osteoperosis?
Bone density is reduced due to osteoclast activity being higher than osteoblast activity, produces holes that can’t be filled by the osteoblasts so there are large gaps between the trabeculae.
What does loss of mass of the trabeculae in osteoperosis mean?
Susceptible to fracture as bone no longer provides adequate mechanical support.
What is type 1 osteoperosis, who does it affect and what happens?
Rapidly falling levels of oestrogen after the menopause therefore affects postmenopausal women. Oestrogen usually regulated osteoclast activity by increasing osteoblast activity to keep the ratio balanced. Less oestrogen means that the ratio of activity changes and so the osteoclasts activity increases compared to osteoblast. This means more bone is broken down than is made so there are more gaps between the trabeculae and so the bones become weaker.
What is type 2 osteoperosis and who does it affect?
Reduction in osteoblast function, affects elderly of both sexes.
What are risk factors for osteoperosis?
Age- older, bones start to become thinner and more porous
Gender- women mor likely post menopause
Poor diet- not enough calcium or vit d
Insufficient exercise- immobilisation leads to accelerated bone loss
Smoking
What are some treatments for osteoperosis?
Hormone replacement therapy (for women)
Change in diet/ calcium and vit d supplements
Exercise
Stopping smoking
What can cause osteomalacia?
Inadequate intake of calcium/vit d/phosphate or a combination.
Why is vit d important in bone development?
Involved in absorption of calcium an phosphate by SI. In its absence poorly mineralised matrix known as osteoid is formed and prevents osteoblasts to osteoclasts. bones are unable to support the body weight so bend.
Where is vit d hydrolysed?
First in the liver then again in the kidney, could be deficient if these aren’t working due to liver/kidney disease.
When does osteomalacia occur?
During bone remodelling
